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Title: Tumour growth stimulation following partial hepatectomy in mice is associated with increased upregulation of c-Met.
Austin Authors: Harun, Nadia;Costa, Patricia;Christophi, Christopher 
Affiliation: Department of Surgery, AH/NH Austin Hospital, University of Melbourne, Heidelberg, VIC, 3084, Australia
Issue Date: 31-Jul-2013
Publication information: Clinical & Experimental Metastasis 2013; 31(1): 1-14
Abstract: Hepatic resection is the preferred option for curative treatment of colorectal liver metastasis (CLM). However, this is associated with significant recurrence rates in both hepatic and extrahepatic sites. The upregulation of growth factors required for liver regeneration after resection is thought to stimulate the growth of micrometastases. The current study describes temporal changes in the expression of hepatocyte growth factor receptor (c-Met), epidermal growth factor receptor (EGFR) and insulin growth factor I receptor (IGF-IR) in an orthotopic mouse model of liver resection and tumour induction. Mice underwent 70% hepatectomy and induction of liver metastases through intrasplenic injection of colorectal cancer cells. Control groups included sham-operated mice and 70% hepatectomy alone. The expression levels of liver and tumour c-Met, EGFR and IGF-IR were quantified by quantitative RT-PCR at different time points. 70% liver resection stimulates tumour growth; increases the expression of c-Met within established tumours and surrounding liver parenchyma; downregulates EGFR expression and increases IGF-IR expression within the liver parenchyma. In conclusion, we demonstrate in our mouse model that major hepatectomy stimulates engraftment and growth of CLM and that this effect is probably due to the upregulation of c-Met as a result of the liver regeneration process. Liver IGF-IR may also contribute to this phenomenon through a paracrine effect on tumour growth. This study provides support for the role of c-Met in the stimulation of tumour growth after resection possibly through the promotion of tumour cell proliferation.
Gov't Doc #: 23900501
DOI: 10.1007/s10585-013-9604-7
Journal: Clinical & experimental metastasis
Type: Journal Article
Subjects: Animals
Cell Proliferation
Colorectal Neoplasms.metabolism.pathology
Disease Models, Animal
Insulin-Like Growth Factor I.biosynthesis
Liver Regeneration.physiology
Mice, Inbred CBA
Proto-Oncogene Proteins c-met.biosynthesis
RNA, Messenger.analysis
Receptor, Epidermal Growth Factor.biosynthesis
Reverse Transcriptase Polymerase Chain Reaction
Appears in Collections:Journal articles

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